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Published on: October 25, 2018
Effect of complement and its regulation on myasthenia gravis pathogenesis
Linda L Kusner1, Henry J Kaminski, Jindrich Soltys
1Department of Neurology & Psychiatry, Saint Louis University, 1438 South Grand Blvd, St Louis, MO 63104, USA. lkusner@slu.edu
Expert Review of Clinical Immunology
|May 19, 2010
Summary
Myasthenia gravis involves antibodies attacking acetylcholine receptors, causing muscle weakness. Complement-mediated lysis is the main cause of neuromuscular junction damage, suggesting complement inhibitors as a potential therapy.
Area of Science:
- Immunology
- Neuroscience
- Pathology
Background:
- Myasthenia gravis (MG) is an autoimmune disorder characterized by antibodies targeting the skeletal muscle acetylcholine receptor.
- Antibody binding can impair neuromuscular transmission via receptor blockade or modulation.
- Complement-mediated lysis of the postsynaptic membrane is the primary mechanism of neuromuscular junction injury in MG.
Purpose of the Study:
- To review the central role of complement in experimentally acquired MG (EAMG) and human MG pathogenesis.
- To explore the emerging role of complement in T- and B-cell function.
- To discuss the therapeutic potential of complement inhibitors for human MG.
Main Methods:
- Review of existing literature on complement's role in EAMG and MG.
- Analysis of studies investigating complement's involvement in immune cell function.
- Evaluation of data supporting complement inhibitor-based therapies.
Main Results:
- Complement plays a critical role in the pathogenesis of EAMG and human MG.
- Complement influences T- and B-cell functions relevant to MG.
- Experimental evidence supports the efficacy of complement inhibition in EAMG models.
Conclusions:
- Complement-mediated lysis is the predominant mechanism causing neuromuscular junction damage in MG.
- Targeting the complement system offers a promising therapeutic strategy for human MG.
- Further research into complement pathways could lead to novel treatments for myasthenia gravis.
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